Thread by @strain_rate

🧵Strain is defined in three dimensions; longitudinal, circumferential and transmural (radial). Each strain component defines deformation in one dimension. It is, however, absurd to consider the three components independently, or as reflection of shortening of specific fibres.

1/ Any three-dimensional object is defined by a three dimensional coordinate system. The simplest is the cartesian system of xyz. In the LV myocardium, being more of a a hollow ellipsoid, the longitudinal, circumferential and transmural directions are more convenient.

2/ Thus, systolic deformation of a 3D object occurs along the three axes, simultaneously. With some incompressibility (not necessarily total), deformation in one direction must relate to deformation in the two other, expansion in one usually follows shrinking in the two others.

3/ Longitudinal strain has been the subject of a recent thread. Even if there is no basic definition, all instances are longitudinal shortening, which means negative strain as the wall becomes shorter: Sl = (L -L0)/L0 = (Ls - Ld) / Ld

4/ Given any degree of incompressibility, if the wall shortens, it has to thicken. Wall thickening is in the transmural direction, transmural strain is simply relative wall thickening. Wall thickening is thus largely a function of wall shortening.

Wall thickening occurs in the transmural direction, so transmural strain is nothing more than relative wall thickening: St = (WTs - WTd) / WTd, which is positive as the wall becomes thicker in systole. It can be estimated by M-mode:

6/ Thus, transmural strain should be on the order of 50%, as known from M-mode studies. Using speckle tracking the tracking is vulnerable to reduced lateral resolution. As lateral resolution decreases with depth, transmural strain cannot be estimated from apical views

7/ In transverse views, lateral tracking is poorer than vertical, in addition the values are smoothed, giving low values all over as in this example.

7/Firstly, there are no transmural fibres, and secondly if there had been, shortening would not result in wall thickening. Wall thickening is mainly a function of wall shortening and myocardial volume conservation (partial or total incompressibility).

8/ so what about circumferential strain? In systole, the outer diameter, and hence, circumference decreases somewhat, about 12 - 13%, we found in he HUNT study pubmed.ncbi.nlm.nih.gov/31673384/ This must be a measure of circumferential fibre shortening, geometric change cannot explain that

9/But as the wall thickens, midwall and inner lines move inwards, inner more than midwall. There would have been circumferential strain due to thickening of longitudinal fibres, even without circumferential fibres if there was pericardial restraint.

There is a gradient of strain from the outer to the inner circumference, as we did show pubmed.ncbi.nlm.nih.gov/31673384/
The gradients of strain will be subject of another thread.

11/ So circumferential strain is shortening, i.e. negative. But as circumference is Pi x D, so circumferential strain is equal to the shortening of the corresponding diameter, and circumferential strain is the negative value of fractional shortening.

12/ But this means that fractional shortening actually is circumferential, not transverse (radial) deformation, the true radial deformation is wall thickening. This is shown here: thicker wall will give reduced wall thickening (radial function), but increased FS.

13/ And the take home message: The three strain components have nothing to do with *selective* fibre function. They are the three spatial coordinates of ONE deformation of ONE object, the LV myocardium, and the summed function of ALL fibre shortenings.

14 / As there is very little myocardial compressibility, pubmed.ncbi.nlm.nih.gov/32978265/, the three strain components are very inter related, and longitudinal strain (if any) should be sufficient for global function